Neurotrophin‐3 stimulates stem Leydig cell proliferation during regeneration in rats

Yu, Yige; Li, Zengqiang; Ma, Feifei; Chen, Quanxu; Lin, Liben; Xu, Qiang; Li, Yang; Xin, Xiu; Pan, Peipei; Huang, Tongliang; Wang, Yiyan; Fei, Qianjin

doi:10.1111/jcmm.15886

Cited by 8 publications

(6 citation statements)

References 47 publications

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“…After being blocked with 5% BSA in TBST for 2 h, the membrane was incubated overnight at 4°C with primary antibody against the following antigens: LHCGR (1:1000), SCARB1(1:1000), STAR (1:1000), CAT (1:1000), INSL3 (1:1000), HSD3B1 (1:1000), CYP11A1 (1:1000), SRD5A1 (1:1000), AKR1C14 (1:1000), SOD1 (1:1000), SOD2 (1:1000), STAT3 (1:1000), pSTAT3 (1:1000), and RPS16 (1:1000), respectively. These antibodies were verified in the previous studies 16–18 . The membrane was then washed three times and incubated with HRP‐conjugated anti‐rabbit or anti‐goat IgG secondary antibody (1:2000, Bioword, USA) for 2 h at room temperature and washed three times.…”

Section: Methodsmentioning

confidence: 80%

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Oncostatin M stimulates immature Leydig cell proliferation but inhibits its maturation and function in rats through JAK1/STAT3 signaling and induction of oxidative stress in vitro

Tian

Wang

et al. 2021

Andrology

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Background : Oncostatin M (OSM) is a member of the interleukin‐6 group of cytokines, which can regulate cell proliferation, growth, and function. Immature Leydig cells have the ability to proliferate and differentiate, and adult Leydig cells have the function of testosterone synthesis. However, the role and underlying mechanisms of OSM on the proliferation and function of Leydig cells remain unclear. Methods : The effects of OSM on the proliferation, apoptosis, and function of immature Leydig cells isolated from 35‐day‐old rats and the function of adult Leydig cells isolated from 63‐day‐old rats in vitro. Results : OSM stimulated immature Leydig cell proliferation after up‐regulating the expression of Ccnd1 and Cdk4 to drive the transition of G1 phase to M2 phase in the cell cycle at 10 and 100 ng/ml. OSM did not affect the apoptosis of immature Leydig cells up to 100 ng/ml. OSM inhibited testosterone production in immature and adult Leydig cells by down‐regulating the expression of Lhcgr, Star, Cyp11a1, Hsd3b1, and Cyp17a1 at 1–100 ng/ml. OSM induced reactive oxygen species and down‐regulated the expression of antioxidant genes and lowered mitochondrial membrane potential at 10 and 100 ng/ml in both Leydig cells. Janus kinase 1 (JAK1) antagonist filgotinib and signal transducer and activator of transcription 3 (STAT3) antagonist S3I‐201 reversed the effect of OSM, indicating that it acts on JAK1/STAT3 signaling. Conclusion : Oncostatin M stimulates immature Leydig cell proliferation while inhibiting the function of immature and adult Leydig cells.

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Section: Methodsmentioning

confidence: 80%

“…These antibodies were verified in the previous studies. [16][17][18] The membrane was then washed S2.…”

Section: Western Blottingmentioning

confidence: 99%

Oncostatin M stimulates immature Leydig cell proliferation but inhibits its maturation and function in rats through JAK1/STAT3 signaling and induction of oxidative stress in vitro

Tian

Wang

et al. 2021

Andrology

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“…MDK is a heparin-binding growth factor expressed abundantly in ovarian follicles and promotes the cytoplasmic maturation of oocytes ( 44 , 59 ). NTF3 is a member of the NGF family involved in tissue development and stimulates Leydig cell proliferation ( 60 ). Also, it has been involved in the direct control of ovarian function, including follicle assembly, activation of the primordial follicles, follicular growth and development, oocyte maturation, steroidogenesis, ovulation, and corpus luteum formation ( 46 ).…”

Section: Discussionmentioning

confidence: 99%

Shuttle Transfer of mRNA Transcripts via Extracellular Vesicles From Male Reproductive Tract Cells to the Cumulus–Oocyte Complex in Rabbits (Oryctolagus cuniculus)

et al. 2022

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Semen is known to contain an ovulation-inducing factor (identified as a nerve growth factor, NGF) that shows a significant increase in ovulation after semen deposition in induced ovulatory species. However, the interplay between the male reproductive tract cells and oocyte maturation through messenger RNA (mRNA) cargo is yet to be investigated. Extracellular vesicles (EVs) from the primary culture of rabbit prostate (pEVs), epididymis (eEVs), and testis (tEVs) were isolated to examine their contents for several mRNA transcripts through relative quantitative PCR (RT-qPCR). The expressions of NGF, neurotrophin (NTF3), vascular endothelial growth factor A (VEGFA), A disintegrin and metalloprotease 17 (ADAM17), midkine (MDK), kisspeptin (KISS1), and gonadotrophin-releasing hormone (GNRH1) were examined in isolated EVs. EVs were characterized through transmission electron microscopy. EV uptake by cumulus cell culture was confirmed through microscopic detection of PKH26-stained EVs. Furthermore, the effects of pEVs, eEVs, and tEVs were compared with NGF (10, 20, and 30 ng/ml) supplementation on oocyte in vitro maturation (IVM) and transcript expression. KISS1, NTF3, MDK, ADAM17, GAPDH, and ACTB were detected in all EV types. GNRH1 was detected in tEVs. NGF was detected in pEVs, whereas VEGFA was detected in eEVs. pEVs, eEVs, and 20 ng/ml NGF showed the highest grade of cumulus expansion, followed by tEVs and 10 ng/ml NGF. Control groups and 30 ng/ml NGF showed the least grade of cumulus expansion. Similarly, first polar body (PB) extrusion was significantly increased in oocytes matured with eEVs, pEVs, tEVs, NGF20 (20 ng/ml NGF), NGF10 (10 ng/ml NGF), control, and NGF30 (30 ng/ml NGF). Additionally, the expression of NGFR showed a 1.5-fold increase in cumulus cells supplemented with eEVs compared with the control group, while the expression of PTGS2 (COX2) and NTRK showed 3-fold and 5-fold increase in NGF20-supplemented cumulus-oocyte complexes (COCs), respectively. Oocyte PMP15 expression showed a 1.8-fold increase in IVM medium supplemented with eEVs. Additionally, oocyte NGFR and NTRK expressions were drastically increased in IVM medium supplemented with pEVS (3.2- and 1.6-fold, respectively) and tEVs (4- and 1.7-fold, respectively). This is the first report to examine the presence of mRNA cargo in the EVs of male rabbit reproductive tract cells that provides a model for the stimulation of female rabbits after semen deposition.

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“…Hearts from mice in each group (4 samples, 4 biological replicates per group) were prepared as previously described. 32 The MYL7 primary antibody (17283–1‐AP, Proteintech, 1:1000) and HRP secondary antibody (AS014, ABclonal, 1:1000) were used. Relative MYL7 expression was calculated as integrated optical density (IOD)/area by using a quantitative digital image analysis system (Image‐Pro Plus 6.0).…”

Section: Methodsmentioning

confidence: 99%

Vasorin deficiency leads to cardiac hypertrophy by targeting MYL7 in young mice

Guo

Liang

et al. 2021

J Cellular Molecular Medi

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Vasorin (VASN), also known as SLIT-like 2 (slitl2), is a 673-amino acid transmembrane glycoprotein localized on the cell surface 1 that is cleaved by a disintegrin and metalloproteinase. VASN is considered a potential biomarker and therapeutic target for cancer. 2,3 Notably, VASN is highly conserved in many organs from embryonic development to adulthood. 4,5 There is limited literature on VASN function.In embryonic development, VASN is primarily expressed in the heart and lungs. 1 VASN is expressed in vascular smooth muscle cells 1 and

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Neurotrophin‐3 stimulates stem Leydig cell proliferation during regeneration in rats

Abstract: This is an open access article under the terms of the Creative Commons Attribution License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited.

Cited by 8 publications

References 47 publications

Oncostatin M stimulates immature Leydig cell proliferation but inhibits its maturation and function in rats through JAK1/STAT3 signaling and induction of oxidative stress in vitro

Oncostatin M stimulates immature Leydig cell proliferation but inhibits its maturation and function in rats through JAK1/STAT3 signaling and induction of oxidative stress in vitro

Shuttle Transfer of mRNA Transcripts via Extracellular Vesicles From Male Reproductive Tract Cells to the Cumulus–Oocyte Complex in Rabbits (Oryctolagus cuniculus)

Vasorin deficiency leads to cardiac hypertrophy by targeting MYL7 in young mice

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